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15 rezultatima
Toxicity of the cyanobacterial neurotoxin beta-N-methylamino-L-alanine to three aquatic animal species.
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Beta-N-methylamino-L-alanine (BMAA), a neurotoxin and candidate contributory cause of neurodegenerative diseases including amyotrophic lateral sclerosis, is produced by aquatic and terrestrial cyanobacteria. We have determined BMAA toxicity to three aquatic animal species: zebra fish (Danio rerio),
beta-Cyano-L-alanine toxicity: evidence for the involvement of an excitotoxic mechanism.
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The legume Vicia sativa (common vetch) harbors the neurotoxic nonprotein amino acid beta-cyano-L-alanine (BCLA) and its gamma-glutamyl derivative. BCLA elicits hyperexcitability, convulsions, and rigidity in chicks and rats after oral or intraperitoneal administration, but the mechanism of its
Effects of the cyanobacterial neurotoxin beta-N-methylamino-L-alanine on the early-life stage development of zebrafish (Danio rerio).
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beta-N-Methylamino-L-alanine (BMAA), a neurotoxic amino acid, is produced by members of all known groups of cyanobacteria. In the presence of added carbonate, BMAA generates an analogue of glutamate which has been associated with motor neuron (MN) diseases via a mechanism of motor neurone specific
Isolated deficiency of glucocorticoids presenting with cholestasis.
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BACKGROUND
Isolated deficiency of glucocorticoids is characterized by elevated levels of adrenocorticotropin (ACTH) and normal aldosterone production. It is rare for isolated deficiency of glucocorticoids to be associated with liver involvement. A case of an infant with isolated deficiency of
Marked stereospecificity in a new class of anticonvulsants.
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N-Acetyl-D,L-alanine-N-benzylamide and N-acetyl-D,L-phenylglycine-N-benzylamide are two novel anticonvulsants that selectively blocked maximal electric shock-induced tonic extensor seizures in mice. For both compounds, the anticonvulsant activity is due to the D-stereoisomer, and the L-stereoisomer
Effect of structural modification of the hydantoin ring on anticonvulsant activity.
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Selectively substituted hydantoins 1 (15 examples), 4-hydroxy-2-imidazolidinones 2 (13 examples), 2-imidazolones 3 (10 examples), 2-imidazolidinones 4 (four examples), vicinal diamines 5 (two examples), and simple amino acid derivatives 6 (four examples) have been prepared and evaluated in the
L-beta-methylamino-alanine-induced behavioral changes in rats.
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L-beta-N-methylamino-L-alanine (L-BMAA, 500 micrograms) infusions into the lateral ventricle induced splay, clonic convulsions, and rigidity in about 60% of rats. Electroencephalograph (EEG) recording during clonic convulsions and rigidity demonstrated epileptiform discharges. Duration and severity
Specific antagonism of behavioral action of "uncommon" amino acids linked to motor-system diseases.
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Beta-N-methylamino-L-alanine (BMAA) and beta-N-oxalylamino-L-alanine (BOAA) are chemically related amino acids present in the seeds of Cycas circinalis and Lathyrus sativus, respectively. Consumption of these seeds has been linked to Guam amyotrophic lateral sclerosis (BMAA) and lathyrism (BOAA; a
Drug reaction with eosinophilia and systemic symptoms syndrome probably induced by a lamotrigine-ginseng drug interaction.
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The likelihood of a drug reaction with lamotrigine is increased by dose escalation that is too rapid or drug interactions that increase the concentration of lamotrigine. There is a well-documented interaction between valproic acid and lamotrigine in which lamotrigine levels are increased,
A case of lacosamide-induced hepatotoxicity.
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BACKGROUND
Lacosamide is a novel antiepileptic drug that acts mainly via the selective enhancement of slow inactivation of voltage-gated sodium channels. It has been reported that lacosamide is effective and generally tolerable as an adjuvant treatment in patients with partial seizures. There are
Effect of L-cycloserine on brain GABA metabolism.
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The administration of L-cycloserine to mice resulted in a dramatic decrease in the activities of 4-aminobutyrate:2-oxoglutarate aminotransferase (GABA-T) and L-alanine:2-oxoglutarate aminotransferase (ALA-T) in both brain and liver. L-Aspartate:2-oxoglutarate aminotransferase was inhibited only
The correlation of dystonia severity and serum transaminases in a child with a brain injury.
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BACKGROUND
Severe anoxic brain injury can lead to prolonged episodes of status dystonicus. Sustained dystonia can result in skeletal muscle breakdown and elevation of serum transaminases, which can initially be confused with polypharmacy-related hepatotoxicity or an underlying metabolic
Carbamoylphosphate synthetase deficiency in an adult: deterioration due to administration of valproic acid.
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A 24-year-old patient had symptoms of lethargy, convulsions and hyperammonaemia during valproic acid therapy. Cessation of valproic acid treatment brought about an improvement both of the symptoms and of the hyperammonaemia. However, enzymatic analysis after the cessation of valproic acid therapy
Glycine modulates the toxicity of benzyl acetate in F344 rats.
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The influence of supplemental glycine on benzyl acetate (BA; a compound metabolized via the hippurate pathway)-induced toxicity was investigated. Groups of male F344 rats were fed NIH-07 diet containing 0, 20,000, 35,000, or 50,000 ppm BA for up to 28 days. Two additional groups were fed NIH-07 diet
Discovery and partial characterization of primate motor-system toxins.
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beta-N-Oxalylamino-L-alanine (BOAA) and beta-N-methylamino-L-alanine (BMAA) are chemically related excitant amino acids isolated from the seed of Lathyrus sativus (BOAA) and Cycas circinalis (BMAA), consumption of which has been linked to lathyrism (an upper motor neuron disorder) and Guam
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